Gene expression profiling was performed in ccRCC cells, which either express both HIF1alpha and HIF2alpha (either naturally or by virtue of induced expression of HIF1alpha) or express HIF2alpha alone (either naturally or by virtue of a HIF1alpha shRNA), to identify genes regulated by HIF1alpha in ccRCC cells.
Genetic and functional studies implicate HIF1α as a 14q kidney cancer suppressor gene.
Specimen part, Cell line
View SamplesThe effects of constitutively active Hypoxia Inducible Factor (HIF) and inactivated von Hippel-Lindau tumor suppressor gene product (pVHL) were examined in a mouse model. Conditionally expressed, constitutively active HIF-1a and HIF-2a were compared with inactivated pVHL.
Failure to prolyl hydroxylate hypoxia-inducible factor alpha phenocopies VHL inactivation in vivo.
Specimen part
View SamplesThe roles of histone demethylase RBP2 in gene expression were assessed using gene expression profiling experiments with wild type and RBP2-/- primary MEFs. Several cytokine genes including SDF1 and Kit ligand were upregulated upon inactivation of RBP2.
The retinoblastoma binding protein RBP2 is an H3K4 demethylase.
No sample metadata fields
View SamplesmRNA expression was assayed from T47D SCR and T47D EGLN2 conditional knock down cell lines in order to profile the gene expression pattern regulated by EGLN2.
Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
EglN2 associates with the NRF1-PGC1α complex and controls mitochondrial function in breast cancer.
Specimen part, Cell line
View SamplesIn order to perform integrated analysis for EglN2 ChIP-Seq and microarray to identify EglN2 direct target genes, we performed the microarray analysis for T47D breast cancer cells with either control or EglN2 siRNA followed by hypoxia+DMOG treatment
EglN2 associates with the NRF1-PGC1α complex and controls mitochondrial function in breast cancer.
Specimen part, Cell line
View SamplesComparison of ccRCC cells with high HIF or low HIF activity Overall design: Cells expressing control (VEC) were compared to cells with ARNT1 loss using sh/sgRNA targeting ARNT1 The samples labeled 'con' are parental Vhl-null cells and represent the 'high HIF' state. The other 2 cell lines represent the 'low HIF' state. The cell line labeled shArnt have loss of a protein named ARNT by virtue of RNAi-mediated knockdown using a shRNA targeting ARNT. The sample labeled lcARNT has loss of ARNT protein using a lenti-crispr mediated sgRNA.
HIF activation causes synthetic lethality between the <i>VHL</i> tumor suppressor and the <i>EZH1</i> histone methyltransferase.
No sample metadata fields
View SamplesWe report that Dnmt1 is crucial during perinatal intestinal development. Loss of Dnmt1 in intervillus progenitor cells causes global hypomethylation, DNA damage, premature differentiation, and apoptosis, and consequently, loss of nascent villi. We further confirm the critical role for Dnmt1 during crypt development using the in vitro organoid culture system, and illustrate a clear differential requirement for Dnmt1 in immature versus mature organoids. These results demonstrate an essential role for Dnmt1 in maintaining genomic stability during intestinal development and the establishment of intestinal crypts. Overall design: We performed RNA-Seq of control and Dnmt1-ablated intestinal progenitor cells isolated from parrafin embedded tissues by laser capture microdissection (LCM).
Dnmt1 is essential to maintain progenitors in the perinatal intestinal epithelium.
No sample metadata fields
View SamplesThe menin tumor suppressor protein (Men1) is deficient in many endocrine tumors and forms an active complex with MLL family histone methyltransferases. This Men1 complex promotes histone H3 lysine 4 trimethylation at target loci including homeobox genes and cyclin-dependent kinase inhibitor genes. The loss of Men1 may be tumorigenic because it leads to decreased histone H3 lysine 4 trimethylation resulting in expressional changes of specific genes.
Loss of the retinoblastoma binding protein 2 (RBP2) histone demethylase suppresses tumorigenesis in mice lacking Rb1 or Men1.
No sample metadata fields
View SamplesAberrations in epigenetic processes, such as histone methylation, can lead to cancer. Retinoblastoma Binding Protein 2 (RBP2)(also called JARID1A or KDM5A) can demethylate tri- and di-methylated lysine 4 in histone H3, which are epigenetic marks for transcriptionally active chromatin, whereas the MEN1 tumor suppressor promotes H3K4 methylation. Previous studies suggested that inhibition of RBP2 contributed to tumor suppression by pRB. Here we show RBP2 loss promotes cellular differentiation in vitro. We use mouse expression array 430 2.0 array to profile gene expression patterns of Rbp2f/f and Rbp2-/- ES cells in ES cell medium and after 6 days in ES cell medium without LIF.
Loss of the retinoblastoma binding protein 2 (RBP2) histone demethylase suppresses tumorigenesis in mice lacking Rb1 or Men1.
Specimen part
View Samples